Descending facilitation of spinal NMDA-dependent reflex potentiation from pontine tegmentum in rats

This study was conducted to investigate whether dorsolateral pontine tegmentum stimulation modulates spinal reflex potentiation (SRP) and whether serotonergic neurotransmission is involved in such a modulation. Reflex activities of the external urethra sphincter (EUS) electromyogram in response to a test stimulation (TS; 1/30 Hz) or repetitive stimulation (RS; 1 Hz) on the pelvic afferent nerve in 35 anesthetized rats were recorded with/without synchronized train pontine stimulation (PS; 300 Hz, 30 ms) and/or intrathecal administrations of 10 μl of 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo (F) quinoxaline (NBQX; 100 μM), d-2-amino-5-phosphonovalerate (APV; 100 μM), N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]- N-(2-pyridinyl) cyclohexanecarboxamide trihydrochloride (WAY 100635; 100 μM), and 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT; 100 μM). The TS evoked a single action potential (1.00 ± 0.00 spikes/stimulation), while the RS produced a long-lasting SRP (16.12 ± 1.59 spikes/stimulation) that was abolished by APV (1.57 ± 0.29 spikes/stimulation) and was attenuated by NBQX (7.42 ± 0.57 spikes/stimulation). Synchronized train PS with RS (PS+RS) produced facilitation in RS-induced SRP (25.17 ± 2.21 spikes/stimulation). Intrathecal WAY 100635 abolished the facilitation in SRP as a result of the synchronized PS (14.66 ± 1.58 spikes/stimulation). On the other hand, intrathecal 8-OH-DPAT elicited facilitation in the RS-induced SRP (25.16 ± 1.05 spikes/stimulation) without synchronized PS. Our findings suggest that dorsolateral pontine tegmentum may modulate N-methyl-d-aspartic acid-dependent SRP via descending serotonergic neurotransmission. This descending modulation may have physiological/pharmacological relevance in the neural controls of urethral closure.

Effects of Paired and Unpaired Eye-Blink Conditioning on Purkinje Cell Morphology

This experiment addressed (1) the importance of conjunctive stimulus presentation for morphological plasticity of cerebellar Purkinje cells and inhibitory interneurons and (2) whether plasticity is restricted to the spiny branches of Purkinje cells, which receive parallel fiber input. These issues were investigated in naive rabbits and in rabbits that received paired or unpaired presentations of the conditioned stimulus (CS) and unconditioned stimulus (US). To direct CS input to the cerebellar cortex, pontine stimulation served as the CS. Air puffs to the cornea served as the US. Paired condition rabbits received pontine stimulation for 350 msec paired with a coterminating 100-msec air puff. Unpaired condition rabbits received the same stimuli in a pseudorandom order at 1- to 32-sec intervals. Rabbits were trained for a mean of 12 days. Naive rabbits received no treatment. In Golgi-stained Purkinje neurons in lobule HVI, total dendritic length, main branch length, total spiny branch length, and number of spiny branch arbors were all greater in the naive group than in the paired and unpaired groups, which did not differ. No differences were found between the hemispheres ipsilateral and contralateral to the trained eye. The dendritic length and number of branches for inhibitory interneurons did not differ across groups. The Purkinje cell morphological changes detected with these methods do not appear to be uniquely related to the conjunctive activation of the CS and US in the paired condition.

Reticulospinal Systems Mediate Atonia With Short and Long Latencies

Kohyama, Jun, Yuan-Yang Lai, and Jerome M. Siegel. Reticulospinal systems mediate atonia with short and long latencies. J. Neurophysiol. 80: 000–000, 1998. The pontomedullary region is responsible for both the tonic and phasic reduction of muscle activity in rapid-eye-movement sleep and contributes to the control of muscle tone in waking. This study focused on determining the time course of activity in the pontomedullary systems mediating atonia. Short-train stimulations (3 0.2-ms pulses at 330 Hz) of the pons and medulla suppressed neck and hindlimb muscle activity in decerebrate cats. We identified two distinct phases of suppression, early and late. The anatomic sites that produced each suppression were intermixed. We estimated the dividing value of the conduction velocity for reticulospinal projections responsible for early and late phases of hindlimb muscle tone suppression to be 22.8 m/s. In the medial medulla, 238 reticulospinal units, which send axons to the L1 level of the spinal cord, were identified. Pontine stimulation that suppressed hindlimb muscle tone increased the firing rate of 138 units (type I). Sixteen type I units showed a delayed response to the pontine stimulation with a latency of 10 ms or longer (type Id), whereas 122 type I units exhibited an earlier response (type Ie). Seven type Ie units had an axonal conduction velocity of <22.8 m/s, whereas the remaining 115 conducted at faster than 22.8 m/s. Early and late hindlimb muscle tone suppressions were hypothesized to be mediated through fast and slow conducting type Ie reticulospinal units. The activity of type Id neurons may contribute to the cessation of the early-phase suppression as well as to the induction, maintenance, or cessation of the late-phase suppression.

Eye movements induced by pontine stimulation: interaction with visually triggered saccades

1. Rhesus monkeys were trained to look to brief visual targets presented in an otherwise darkened room. On some trials, after the visual target was extinguished but before a saccade to it could be initiated, the eyes were driven to another orbital position by microstimulation of the paramedian pontine reticular formation. If, as current models of the saccadic system suggest, a copy of the motor command is used as a feedback signal of eye position, failure to compensate for stimulation-induced movements would indicate that stimulation occurred at a site beyond the point from which the eye position signal was derived. 2. Animals compensated for perturbations of eye position induced by stimulation of most pontine sites by making saccades that directed gaze to the position of the visual target. With stimulation at other pontine sites, compensatory saccades did not occur. 3. Pontine stimulation sometimes triggered, prematurely, impending visually directed saccades. The direction and amplitude of the premature movement depended upon the location of the briefly presented visual target. The amplitude of the premature movement was also a function of the interval between the stimulation train and the impending saccade. These data suggest that input signals for the horizontal and vertical pulse/step generators develop gradually during the presaccadic interval. Saccade trigger signals need to be delayed until the formation of these signals is completed. 4. The implications of these findings for models of the saccadic system are discussed. Robinson's local feedback model of the saccadic system can explain compensation for pontine stimulation-induced changes in eye position but cannot easily account for the failure to compensate for perturbations in eye position produced by stimulation at other sites. Modified versions of Robinson's model, which assume that the input signal to the pulse/step generator is the desired displacement of the eye, can account for both compensation and the failure to compensate since two separate neural integrators are employed. However, these models ignore kinematic arguments that commands to the extraocular muscles must specify the absolute position of the eye in the orbit rather than a relative movement from a previous position.